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Tumor inhibiting protein p33ING1b is the key expressive product of inhibitor of growth 1.It plays critical role in cell multiplication ,period control ,senescence ,repair of DNA damage ,apoptosis ,and chroma-tin remodeling.The abnormal expression of p33ING1b is closely related to the occurrence and development of tumor.This paper reviews tumor inhibiting protein p 33ING1b in the research development of tumors in digestive system.
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Objective To discuss the expressions and clinical significance of p53 and p33ING1b in human psoriasis and basal cell carcinoma (BCC). Methods Immunohistochemistry EnVision technique was used to detect the expressions of p53 and p33ING1b in samples of 36 psoriasis vulgaris, 28 BCC and 14 normal skins. Results The expression of p53 increased while p33ING1b had a degressive expression in the control group, the psoriasis group and the BCC group. It was found significant statistical difference between the two groups (all P < 0.05). Prominent positive correlation between p53 and p33ING1b were found in both psoriasis group and BCC group (all P<0.05). Conclusions p53 coacts with p33ING1b at local lesions of abnormal proliferative diseases . It′s one of the most prominent mechanisms contributing to deviant cell proliferation.
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Background and purpose:As a new candidate tumor suppressor gene, p33ING1b has many biological functions. This study was done to investigate its role in the regulation of the proliferation of human colon cancer cell line SW480. Methods:The pcDNA3.1(+)/p33ING1b/SW480 cells were identified by Western blot and S-P immunohistochemical method. In order to elucidate the effect of expression of exogenous p33ING1b gene on the colorectal cancer cell SW480, the proliferation rates were analyzed by growth curves and colony formation assay in soft agar for cells including SW480, pcDNA3.1(+)/p33ING1b/SW480 and pcDNA3.1(+)/SW480. At same time, the apoptotic rate of cells and the cell cycle analysis were also tested by flow cytometry.Furthermore,using western blot analysis,we detected the expression level of the protein p53, p21WAF1,Bax and Bcl-2 in those three group cells, which initially indicate the molecule mechanism of inducing apoptosis by gene p33ING1b. Results:The cell growth rates of SW480 cells transfected with pcDNA3.1 (+)/p33ING1b were slower than those transfected with pcDNA3.1(+) or untransfected.The colony formation efficiency of pcDNA3.1(+)/p33ING1b/SW480 were decreased and the apoptotic rates were increased compared with pcDNA3.1(+)/SW480 and SW480(P0.05). Conclusion:After overexpression of exogenous p33ING1b protein in SW480 cell, there were inhibition of the proliferation rate and induction of apoptosis, the molecular mechanism might be associated with up- regulated expression of Bax and down-regulated expression of Bcl-2 by p33ING1b gene.
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Objective To investigate the p33~ ING1b mRNA level and the relationship to clinical pathological data in primary hepatocellular carcinoma(PHC).Methods Reverse transcriptase-polymerase chain reaction (RT-PCR) method was employed to detect the mRNA level of p33~ ING1b in liver cancer tissues and adjacent tissues of cancer.Results p33~ ING1b mRNA was positive expression in 63.6% (35/55) cancer tissues and 70.9% (39/55) adjacent tissues of cancer.The expression level of p33~ ING1b mRNA in cancer tissues (0.410?0.175) was significantly lower than that in adjacent tissues of cancer (0.529?0.203). The level of p33~ ING1b was significantly associated with pathological grades, lymph node metastasis and envelope infiltration, but not associated with sex, age, tumor size, tumor thrombus or liver cirrhosis.Conclusion The decrease of p33~ ING1b may play an important role in the tumorigenesis and development of PHC, and may be an adjuvant parameter in evaluating tumor differentiation, invasion and prognosis.
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PURPOSE: p33(ING1) seems to be a candidate of novel growth inhibitor as a tumor suppressor gene and plays a critical role in regulation of cell cycle progression and susceptibility to apoptosis. In this study, we investigated p33(ING1) expression pattern in human bladder cancer and normal tissue. MATERIALS AND METHODS: RNA was extracted from 42 bladder cancer specimens and 24 normal bladder mucosa. Expression of p33(ING1) was examined by quantitative RT- PCR in which the ratio to GAPDH, an internal control, was used as a standardized expression value of the p33(ING1). Alterations of p33(ING1) expression between cancer and normal mucosa were compared and interrelationship with stage and grade was analyzed. To detect the mutations in the p33(ING1), PCR-SSCP analysis was also performed. RESULTS: Out of 42 bladder cancer (25 superficial and 17 invasive), 9 were grade I, 23 were grade II, and 10 were grade III. p33(ING1) expression in bladder cancer significantly decreased compared to that in normal bladder mucosa. The ratio of p33(ING1)/ GAPDH was 0.45 +/- 0.13 in bladder cancer, whereas for normal bladder mucosa this ratio was 0.66 +/- 0.17 (p <0.001). However, expression of p33(ING1) was neither correlated with tumor stage nor grade (p=0.489 and p=0.375, respectively). Changes in electrophoretic mobility of PCR-SSCP products were not detected in any of bladder cancers. CONCLUSIONS: These data suggest that decreased expression of p33(ING1) may contribute to the development of bladder cancer in part, even though the gene is mostly preserved. However, considering a discrepancy between the rate of mutation and the decreased expression, further study is warranted to determine the mechanism.
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Humanos , Apoptosis , Ciclo Celular , Genes Supresores de Tumor , Membrana Mucosa , Reacción en Cadena de la Polimerasa , ARN , Neoplasias de la Vejiga Urinaria , Vejiga UrinariaRESUMEN
Objective To investigate the relationship between the p33 ING1b protein expression and differentiated degree in human gastric carcinoma. Methods p33 ING1b protein expression was detected by S-P immunohistochemical method in gastric carcinoma and normal gastric mucous tissues. Results The positive rates of p33 ING1b protein expression were 75% (15/20) in well-differentiated, 55% (11/20) in moderate-differentiated and 15% (3/20) in poor-differentiated gastric carcinoma, respectively. The positive rate of p33 ING1b protein expression in gastric carcinoma was significantly lower than that in normal gastric mucosa (100%, 60/60) (P
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Objective:To investigate the expression of P33~(ING1) protein in oral squamous cell carcinoma(OSCC) and its clinical significance. Methods:All samples of normal and cancer tissues from 30 patients with OSCC were examined for protein expression of P33~(ING1) by SP immunohistochemical staining.Results:The positive rate of P33ING1 in OSCC was 40%, that in normal oral mucosa tissue 100% (P
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Objective:To investigate the influence of p33~ING1b and wt-p53 on the biological activities of pancreatic cancer cells. Methods: Sense and anti-sense cDNAs of p33~ING1b were cloned into pcDNA3 eukaryotic expression vector separately, and the recombinant plasmids were solely or co-transfected with wt-p53 into pancreatic cell line SW1990. Flow cytometry was used to analyze the changes of cell cycle, Western blotting was used to evaluate the expression of p33~ING1b and p53 protein, and MG-P-MY staining was applied to observe cell apoptosis. Results: SW1990 cells solely transfected with sense p33~ING1b plasmid or co-transfected with wt-p53 and sense p33~ING1b plasmid expressed more p33~ING1b and had more apoptosis than the antisense p33~ING1b plasmid and mock transfected cells did (P